Argatroban Research Paper

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Argatroban is a synthetic direct thrombin inhibitor. It binds reversibly to thrombin so it requires to be given as a continuous intravenous infusion. It is metabolized mainly by the liver so it needs dose reduction in liver impairment. Its half-life is moderately extended in renal impairment. The effect of renal impairment on argatroban dosage adjustment is unclear. Some studies which were done on dialysis patients used the same dose in normal renal patients with no additional adverse effects and others used lower doses.(40) Argatroban is highly protein bound so it is not cleared significantly during hemodialysis.
The American College of Chest Physicians guidelines for treatment and prevention of HIT 2012 suggested the use of Argatroban over other non-heparin anticoagulants in HD patients with HITTs.(38) In a research that compared 3 doses of Argatroban in HD patients, the preferred regimen was a 250-µg/kg bolus followed by an infusion of 2 µg/kg/minute at the start of dialysis, with the option of stopping the infusion as early as 1 hour before the end of hemodialysis.(41)
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It prevents fibrin formation in the coagulation pathway via thrombin generation inhibition. It inhibits both factor Xa and IIa (anti-Xa effects >20 times anti-IIa effects). It is more selective in factor Xa inhibition than LMWH. Danaparoid half-life is prolonged in renal impairment; it may be about 30 hours. Dialysis patients treated with a bolus of danaparoid might remain anticoagulated in the inter-dialytic interval, which can be problematic in individuals who no longer have active disease. In patients with serum creatinine ≥2.5 mg/dl, after initial dosing, dose reduction should be done or temporary discontinued to prevent the accumulation of plasma anti-Xa. The drug is

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